title: The renaissance of interferon therapy for the treatment of myeloid malignancies.
abstract: IFNα has been used to treat malignant and viral disorders for more than 25 years. Its efficacy is likely the consequence of its broad range of biologic activities, including direct effects on malignant cells, enhancement of anti-tumor immune responses, induction of proapoptotic genes, inhibition of angiogenesis, and promotion of the cycling of dormant malignant stem cells. Because of the recent development of "targeted" therapies, the use of IFN has been dramatically reduced over the last decade. The increasing awareness of the multistep pathogenesis of many malignancies has suggested, however, that such an approach using target-specific agents is not universally effective. These observations have resulted in a number of recent clinical trials utilizing IFNα in patients with chronic myeloid leukemia (CML), systemic mast cell disease, hypereosinophilic syndrome and the Philadelphia chromosome-negative myeloproliferative neoplasms (MPN) with promising outcomes. These reports provide evidence that IFNα, alone or in combination with other agents, can induce surprisingly robust molecular response rates and possibly improve survival. Although IFNα at present remains an experimental form of therapy for patients with myeloid malignancies, these promising results suggest that it may become again an important component of the therapeutic arsenal for this group of hematologic malignancies.
authors.affiliation: Hôpital Saint-Louis, Assistance Publique-Hôpitaux de Paris, Paris, France. jean-jacques.kiladjian@sls.aphp.fr
authors.forename: Jean-Jacques
authors.initials: JJ
authors.lastname: Kiladjian
authors.forename: Ruben A
authors.initials: RA
authors.lastname: Mesa
authors.forename: Ronald
authors.initials: R
authors.lastname: Hoffman
mesh_terms: D017209:Apoptosis / Q000187:drug effects / Q000235:genetics; D001549:Benzamides; D049109:Cell Proliferation / Q000187:drug effects; D002986:Clinical Trials as Topic; D019337:Hematologic Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000276:immunology / Q000473:pathology; D006412:Hematopoietic Stem Cells / Q000187:drug effects / Q000473:pathology; D006801:Humans; D017681:Hypereosinophilic Syndrome / Q000188:drug therapy; D000068877:Imatinib Mesylate; D007370:Interferon Type I / Q000494:pharmacology / Q000627:therapeutic use*; D007951:Leukemia, Myeloid / Q000188:drug therapy; D008415:Mastocytosis / Q000188:drug therapy; D014411:Neoplastic Stem Cells / Q000187:drug effects / Q000473:pathology; D009389:Neovascularization, Pathologic / Q000517:prevention & control; D010879:Piperazines / Q000627:therapeutic use; D011087:Polycythemia Vera / Q000188:drug therapy; D055728:Primary Myelofibrosis / Q000188:drug therapy; D011743:Pyrimidines / Q000627:therapeutic use; D011994:Recombinant Proteins; D013920:Thrombocythemia, Essential / Q000188:drug therapy
chemical_list: D001549:Benzamides; D007370:Interferon Type I; D010879:Piperazines; D011743:Pyrimidines; D011994:Recombinant Proteins; D000068877:Imatinib Mesylate